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Contains fulltext : 244699.pdf (Publisher’s version ) (Open Access) Schizophrenia-spectrum disorders (SSD) are associated with increased inflammatory markers, both in brain and periphery. Augmentation with drugs that lower this pro-inflammatory status may improve clinical presentation. Simvastatin crosses the blood-brain barrier, has anti- inflammatory and neuroprotective effects and reduces metabolic syndrome. In this study, we investigated if 12 months of simvastatin augmentation can improve symptoms and cognition in patients with early SSD. This double-blind placebo-controlled trial included 127 SSD patients across the Netherlands

Conventional antipsychotic medication is ineffective in around a third of patients with schizophrenia, and the nature of the therapeutic response is unpredictable. We investigated whether response to antipsychotics is related to brain glutamate levels prior to treatment. Proton magnetic resonance spectroscopy was used to measure glutamate levels (Glu/Cr) in the anterior cingulate cortex (ACC) and in the thalamus in antipsychotic-naive or minimally medicated patients with first episode psychosis (FEP, n = 71) and healthy volunteers (n = 60), at three sites. Following scanning, patients were treated with amisulpride for 4 weeks (n = 65), then 1H-MRS was repeated (n = 46). Remission status was defined in terms of Positive and Negative Syndrome Scale for Schizophrenia (PANSS) scores. Higher levels of Glu/Cr in the ACC were associated with more severe symptoms at presentation and a lower likelihood of being in remission at 4 weeks (P

Objective: Metabolic syndrome (MS) is highly prevalent in schizophrenia and often a consequence of unhealthy behaviour. Reward-related brain areas might be associated with MS, since they play a major role in regulating health behaviour. This study examined the relationship between MS and brain volumes related to the reward system in schizophrenia. Method: We included patients with schizophrenia, with MS (MS+; n = 23), patients with schizophrenia, without MS (MS−; n = 48), and healthy controls (n = 54). Global brain volumes and volumes of (sub)cortical areas, part of the reward circuit, were compared between patients and controls. In case of a significant brain volume difference between patients and controls, the impact of MS in schizophrenia was examined. Results: Patients had smaller total brain (TB; P = 0.001), GM (P = 0.010), larger ventricles (P = 0.026), and smaller reward circuit volume (P

Considerable uncertainty exists about the defining brain changes associated with bipolar disorder (BD). Understanding and quantifying the sources of uncertainty can help generate novel clinical hypotheses about etiology and assist in the development of biomarkers for indexing disease progression and prognosis. Here we were interested in quantifying case-control differences in intracranial volume (ICV) and each of eight subcortical brain measures: nucleus accumbens, amygdala, caudate, hippocampus, globus pallidus, putamen, thalamus, lateral ventricles. In a large study of 1710 BD patients and 2594 healthy controls, we found consistent volumetric reductions in BD patients for mean hippocampus (Cohen's d=-0.232; P=3.50 × 10(-7)) and thalamus (d=-0.148; P=4.27 × 10(-3)) and enlarged lateral ventricles (d=-0.260; P=3.93 × 10(-5)) in patients. No significant effect of age at illness onset was detected. Stratifying patients based on clinical subtype (BD type I or type II) revealed that BDI patients had significantly larger lateral ventricles and smaller hippocampus and amygdala than controls. However, when comparing BDI and BDII patients directly, we did not detect any significant differences in brain volume. This likely represents similar etiology between BD subtype classifications. Exploratory analyses revealed significantly larger thalamic volumes in patients taking lithium compared with patients not taking lithium. We detected no significant differences between BDII patients and controls in the largest such comparison to date. Findings in this study should be interpreted with caution and with careful consideration of the limitations inherent to meta-analyzed neuroimaging comparisons.Molecular Psychiatry advance online publication, 9 February 2016; doi:10.1038/mp.2015.227. ispartof: Molecular Psychiatry vol:21 issue:12 pages:1710-1716 ispartof: location:England status: published

BackgroundIntellectual deficits are commonly found in schizophrenia patients. These intellectual deficits have been found to be heritable. However, whether the intellectual deficits change over time and, if so, whether the change is related with an increased genetic risk for the disease are not known.MethodWe investigated change of intelligence quotient (IQ) in a twin sample of chronically ill schizophrenia patients, the discordant co-twins and healthy controls during a follow-up period of 5 years. A total of 52 twins completed two IQ assessments: nine patients [three monozygotic (MZ) and six dizygotic (DZ)], 10 unaffected co-twins (three MZ and seven DZ) and 33 healthy control twins (21 MZ and 12 DZ).ResultsA significant interaction effect over time was found between IQ measurement and illness (F=4.22, df=1, pt=2.06, pt=−2.32, pt=−0.49, p=0.63).ConclusionsPatients with schizophrenia in the chronic phase of the disease, but not the discordant co-twins, show a lack of increase in IQ, which is probably due to environmental (non-genetic) factors related to the disease.

The majority of medical disciplines utilize a measurement-based approach for the prevention and early detection of major medical events by monitoring measures that indicate the onset of such an event. However, in psychiatry treatment is often preceded by a major psychiatric crisis or even hospitalization and is followed by a long period of disability and slow recovery. The focus on acute care in psychiatry is due to a lack of valid temporal and objective measures of behavior that translate into day-to-day functioning. Several Behavioral changes in day-to-day functioning are identified as prodromal symptoms for several neuropsychiatric disorders [1,2]. A measurement-based approach is needed in psychiatry to monitor daily functioning and improve patient outcome [3]. Therefore, we have developed a passive behavioral monitoring (PBM) application, called BeHapp (https://behapp.org/), that collects a rich longitudinal trace of real-world social and behavioral data with minimal awareness. PBM is based on the ubiquity of smartphones, and monitors behavior by utilizing the large extend of smartphone sensor modalities available. These modalities allows us to formulate several features related to social behavior, e.g. number of contacts, duration of phone calls, social media usage, and places visited. We studied the predictive power of PBM in differentiating between non-diagnosed controls and neuropsychiatric patients by using smartphone modalities that relate to social behavior. We collected preliminary data from 24 neuropsychiatric patients (9 Major depression, 11 Schizophrenia, 4 Alzheimer’s Disease) and 72 non-diagnosed controls by installing BeHapp on the participant’s own android smartphone. Participants were included over several different ongoing studies and psychiatric screening data was available for 20 non-diagnosed controls. Average participation time was 13.4 days (sd = 5.9), variation is due to early removal of the application. We used GPS, application usage, and WiFi data to generate features that translate into daily social functioning. Simple two-sided t-tests were used to evaluate the difference in means between the neuropsychiatric patient and non-diagnosed control group. Additionally, we applied t-distributed stochastic neighbour embedding clustering [4] to group participants into a two-dimensional space regardless of their diagnosis. Our preliminary results revealed social-behavioral differences between the two groups (pooled patients versus controls) in social media usage; frequency of WhatsApp usage (p Our results suggest that PBM is sensitive in detecting differences in day-to-day social functioning and therefore a potential candidate for a measurement-based approach in psychiatry.

Background and Aims:Neurocognitive and functional neuroimaging studies point to frontal lobe abnormalities in schizophrenia. Molecular and behavioural genetic studies suggest that the frontal lobe is under significant genetic influence. We carried out structural magnetic resonance imaging (MRI) of the frontal lobe in monozygotic (MZ) twins concordant or discordant for schizophrenia and healthy MZ control twins.Methods:The sample comprised 21 concordant pairs, 17 discordant affected and 18 discordant unaffected twins from 19 discordant pairs, and 27 control pairs. Groups were matched on sociodemographic variables. Patient groups (concordant, discordant affected) did not differ on clinical variables. Volumes of superior, middle, inferior and orbital frontal gyri were calculated using the Cavalieri principle on the basis of manual tracing of anatomic boundaries. Group differences were investigated covarying for whole-brain volume, gender and age.Results:Results for superior frontal gyrus showed that twins with schizophrenia (i.e. concordant twins and discordant affected twins) had reduced volume compared to twins without schizophrenia (i.e. discordant unaffected and control twins), indicating an effect of illness. For middle and orbital frontal gyrus, concordant (but not discordant affected) twins differed from non-schizophrenic twins. There were no group differences in inferior frontal gyrus volume.Conclusions:These findings suggest that volume reductions in the superior frontal gyrus are associated with a diagnosis of schizophrenia (in the presence or absence of a co-twin with schizophrenia). On the other hand, volume reductions in middle and orbital frontal gyri are seen only in concordant pairs, perhaps reflecting the increased genetic vulnerability in this group.